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Parkinson's disease stopped in animal model Molecular 'tweezers' break up toxic aggregations of proteins

By Mark Wheeler

(Page 3 of 4)

"We call this unique mechanism 'process-specific,' rather than the common protein-specific inhibition," Bitan added, meaning the compound only attacked the targeted aggregates and nothing else.

The researchers next tried their tweezers in a living animal, the zebrafish, a tropical freshwater fish commonly found in aquariums. The zebrafish is a popular animal for research because it is easily manipulated genetically, develops rapidly and is transparent, making the measurement of biological processes easier.

Using a transgenic zebrafish model for Parkinson's disease, the researchers added CLR01 and used fluorescent proteins to track the tweezer's effect on the aggregations. They found that, just as in cell cultures, CLR01 prevented α-synuclein aggregation and neuronal death, thus stopping the progression of the disorder in the living animal model.

Being able to prevent α-synuclein from aggregating, prevent toxicity and break up existing aggregates is a very encouraging result, but still, at the end of the day, "we've only stopped Parkinson's in zebrafish," Bronstein said.

"Nonetheless," he said, "all of these benefits of CLR01 were found without any evidence of toxicity. And taken together, CLR01 holds great promise as a new drug that can slow or stop the progression of Parkinson's and related disorders. This takes us one step closer to a cure."

The researchers are already studying CLR01 in a mouse model of Parkinson's and say they hope this will lead to human clinical trials.

Other authors of the study included Shubhangi Prabhudesai, Sharmistha Sinha, Aida Attar, Aswani Kotagiri, Arthur G. Fitzmaurice, Ravi Lakshmanan, Magdalena I. Ivanova, Joseph A. Loo and Mark Stahl, all of UCLA, and Frank-Gerrit Klärner and Thomas Schrader of the University of Duisburg–Essen in Germany.

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